Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A 0D model of the Heart

ABSTRACT: A simplified "0D" version of our 3D Cardiac Electromechanical Model based on the Bestel-Clément-Sorine equations of myocardial tissue, Mooney-Rivlin equations of passive material and Windkessel model for cardiac afterload.

SUBMITTER: David Nickerson

PROVIDER: 44c | Physiome Model Repository |

REPOSITORIES: PMR

ACCESS DATA

Json Xml

Publications

Sorry, this publication's infomation has not been loaded in the Indexer, please go directly to PUBMED or Altmetric.

Similar Datasets

The protein expression landscape of the heart across humans and model organisms

Project description:Here we perform a global analysis of cardiac protein expression in humans and model organisms across cardiac chambers using quantitative mass spectrometry based proteomics. We measure >6,500 proteins in each species and create a global comparison of cardiac protein expression across species. The data was collected in an online database for access by cardiac researchers. This data will enable researchers to e. g. choose the best model organism for a scientific question at hand, facilitate transfer of knowledge between studies conducted in different model organisms and help to integrate knowledge of cardiac physiology and disease to point to new leads in cardiac research.

2021-02-03 | PXD012636 | Pride

GNPS - Metabolic reprogramming and membrane glycans remodelling drive zebrafish heart regeneration

Project description:label-free relative quantitation based on nLC-MS/MS performed on heart tissues in a clinically relevant zebrafish model of cardiac tissue regeneration . Each of the six samples (2dp Cl, 2dpS, 7dp Cl, 7dpS, 14dp Cl, 14dpS,) has been analysed in two technical replicates. dpci = days post cryoinjury; dps = days post sham

2022-11-14 | MSV000090703 | GNPS

Transcription profiling of mouse model of heart failure rescued by beta-adrenergic receptor kinase (betaARKct), vs heart failure and untreated samples

Project description:Numerous murine models of heart failure (HF) have been described, many of which develop progressive deterioration of cardiac function. We have recently demonstrated that several of these can be "rescued" or prevented by transgenic cardiac expression of a peptide inhibitor of the beta-adrenergic receptor kinase (betaARKct). To uncover genomic changes associated with cardiomyopathy and/or its phenotypic rescue by the betaARKct, oligonucleotide microarray analysis of left ventricular (LV) gene expression was performed in a total of 53 samples, including 12 each of Normal, HF, and Rescue. Multiple statistical analyses demonstrated significant differences between all groups, and further demonstrated that betaARKct Rescue returned gene expression toward that of Normal. In our statistical analyses, we found that the HF phenotype is blindly predictable based solely on gene expression profile. To investigate the progression of HF, LV gene expression was determined in young mice with mildly diminished cardiac function and in older mice with severely impaired cardiac function. Interestingly, mild and advanced HF mice shared similar gene expression profiles and, importantly, the mild HF mice were predicted as having a HF phenotype when blindly subjected to our predictive model described above. These data not only validate our predictive model, but further demonstrate that, in these mice, the HF gene expression profile appears to already be set in the early stages of HF progression. Thus, we have identified methodologies that have the potential to be used for predictive genomic profiling of cardiac phenotype, including cardiovascular disease.

2007-12-13 | E-GEOD-670 | biostudies-arrayexpress

Heart-on-a-chip model of SARS-CoV-2 infection and treatment with induced pluripotent stem cell derived extracellular vesicles

Project description:Abstract: Although COVID-19–associated heart dysfunction has identified in individuals with SARS-CoV-2 infection, complex and multifaceted pathophysiology in patients complicates the investigation of pathogenesis related to clinical manifestations and mechanisms of cardiac dysfunction after viral invasion. This study comprehensively investigated pathogenesis regarding SARS-CoV-2 infection via tissue model established from human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and cardiomyopathy model induced by angiotensin II. We recapitulated cytopathic features of SARS-CoV-2-induced cardiac damage and monitored the course of cardiac complications after infection, which is critically important to develop therapeutics. We found that SARS-CoV-2 infection of hiPSC-CMs models progressively impaired contractile function and calcium handling and led to cell death. Therapeutics potential towards myocardial injury was further developed in our tissue model. We evaluated cardioprotective effects of extracellular vesicles (EVs) derived from hiPSC source on the infected tissues, indicating that EVs alleviated the impairment of contractile force and cardiac cell death following SARS-CoV-2 infection. We showed that enriched microRNA in hiPSC-EVs can modulate cardiac-specific processes. These findings suggested that cardiac manifestations examined from tissues models provided insights into cardiac injury induced by SARS-CoV-2 infection, and model systems allow the investigation of mechanisms driving cardiac dysfunction and iPSC-EVs served as a promising therapy to rescue cardiac damage from infection.

2022-04-09 | GSE185602 | GEO

Metabolic reprogramming and membrane glycans remodelling drive zebrafish heart regeneration

2022-11-14 | MSV000090703 | MassIVE

Phosphoproteomic analysis of cardiac biowires, cardiac hypertrophy patient explants, and hypertrophic mouse heart

Project description:we apply and evaluate an integrative mass spectrometry-based tissue profiling strategy that allows for a global quantitative phospho-proteomic survey of normal and disease tissue from human, mouse and OOC-derived specimens. The applicability and utility of this approach was tested in the context of fibrotic cardiac tissue samples from Biowire OOC specimens versus cardiac tissue surgical explants from hypertrophic patients and a transaortic constriction mouse pressure-overload model. Unique attributes and phosphorylation signatures specific to each tissue source were identified, but the results clearly showed that clinically-actionable biological inferences are generated by leveraging commonalities exhibited across the compendium. To validate the application of the cross-platform analytical framework, proof of principle drug testing was performed for selection of anti-fibrotic compounds targeting one of the identified fibrosis-related kinases, GSK3, consistent with a role as a key mediator of fibrosis.

2020-07-15 | PXD016492 | Pride

Expression data of the mouse heart of a nose-only HCN inhalation model and a subcutaneous KCN injection model

Project description:Smoke inhalation from a structure fire is a common route of cyanide poisoning in the U.S. Cyanide inhibits cellular respiration, often leading to death. Its rapid distribution throughout the body can result in injuries to multiple organs, and cyanide victims were reported to experience myocardial infarction and other cardiac complications. We performed oligonucleotide microarrays to establish cardiac transcriptomes of an animal model of nose-only inhalation exposure to hydrogen cyanide (HCN), which is relevant to smoke inhalation. We also profiled cardiac transcriptomes after subcutaneous injection of potassium cyanide (KCN). Although the KCN injection model has been often used to evaluate medical countermeasures, this study demonstrated that cardiac transcriptomes are largely different from that of the HCN inhalation model at multiple time points within 24 hours after exposure.

2021-11-02 | GSE158994 | GEO

Heart LC-MS/MS of a primary carnitine deficiency mouse model

Project description:A previous animal model for primary carnitine deficiency (PCD) showed symptoms and died quickly, which did not match the characteristics of patients who remained seemingly asymptomatic for a long time. A new mouse model aimed to simulate the characteristics of seemingly asymptomatic was recently constructed. Possible mechanisms underlying the cardiac phenotype was investigated by proteomics.

2023-06-21 | PXD043158 | Pride

Molecular mechanisms of cannabinoid type II receptor agonists in a mouse model of psychological stress-induced cardiac injury revealed by whole transcriptomic analysis

Project description:To investigate the mechanisms of chronic psychological stress-induced cardiac injury and the protective mechanisms of cannabinoid type II agonists in a model of psychological stress-induced cardiac injury We constructed a mouse chronic psychological stress model based on a chronic unpredictable stress pattern. Mice were randomly divided into control, case (psychological stress group), and treatment groups (post-stress with the cannabinoid type II receptor agonist JWH133) to begin a 3-week psychological stress procedure, and cardiac tissue was subsequently removed for whole-transcriptome sequencing

2022-12-30 | GSE210820 | GEO

scRNA-seq of human engineered heart tissue for analyzing human myocardial fibrosis

Project description:Myocardial infarction models developed to understand fibrosis and promote myocardial regeneration towards ischemic heart disease (IHD) is challenged due to the low-throughput nature of in vivo models and the lack of humanized cardiac scarring in the in vitro models. We generated a novel 4D cardiac scarring model (4DCSM) mimicking the IHD in vitro based on the human engineered heart tissue(hEHT). To identify potential signaling dominating the fibrotic process, we characterized transcriptomics of 4DCSM at different scarring stages by single-cell RNA sequencing. Taken together, our dataset is an informative resource to reveal the critical cell-types fate transformation and in fibrotic process and provides potential comparisons with public clinical data cohorts or other MI fibrosis model data.

2023-06-14 | GSE234714 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data